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lüll Direct activation of human TRPC6 and TRPC3 channels by diacylglycerol Hofmann T; Obukhov AG; Schaefer M; Harteneck C; Gudermann T; Schultz GNature 1999[Jan]; 397 (6716): 259-63Eukaryotic cells respond to many hormones and neurotransmitters with increased activity of the enzyme phospholipase C and a subsequent rise in the concentration of intracellular free calcium ([Ca2+]i). The increase in [Ca2+]i occurs as a result of the release of Ca2+ from intracellular stores and an influx of Ca2+ through the plasma membrane; this influx of Ca2+ may or may not be store-dependent. Drosophila transient receptor potential (TRP) proteins and some mammalian homologues (TRPC proteins) are thought to mediate capacitative Ca2+ entry. Here we describe the molecular mechanism of store-depletion-independent activation of a subfamily of mammalian TRPC channels. We find that hTRPC6 is a non-selective cation channel that is activated by diacylglycerol in a membrane-delimited fashion, independently of protein kinases C activated by diacylglycerol. Although hTRPC3, the closest structural relative of hTRPC6, is activated in the same way, TRPCs 1, 4 and 5 and the vanilloid receptor subtype 1 are unresponsive to the lipid mediator. Thus, hTRPC3 and hTRPC6 represent the first members of a new functional family of second-messenger-operated cation channels, which are activated by diacylglycerol.|Animals[MESH]|CHO Cells[MESH]|Calcium Channels/genetics/*metabolism[MESH]|Calcium/*metabolism[MESH]|Cell Membrane Permeability[MESH]|Cloning, Molecular[MESH]|Cricetinae[MESH]|Diglycerides/*metabolism[MESH]|Enzyme Inhibitors/pharmacology[MESH]|Estrenes/pharmacology[MESH]|Histamine/metabolism[MESH]|Humans[MESH]|Ion Channel Gating[MESH]|Ion Channels/*metabolism[MESH]|Manganese/metabolism[MESH]|Molecular Sequence Data[MESH]|Patch-Clamp Techniques[MESH]|Protein Kinase C/metabolism[MESH]|Pyrrolidinones/pharmacology[MESH]|Second Messenger Systems[MESH]|TRPC Cation Channels[MESH]|TRPC6 Cation Channel[MESH]|Thapsigargin/pharmacology[MESH]|Type C Phospholipases/antagonists & inhibitors/metabolism[MESH] |